A great deal of attention has been devoted to elucidation of the molecular basis of atherogenesis. Five theories have been proposed and supported. It is significant that, in principle, these theories are related: they suggest increased permeability to and entrapment of circulating proliferative and/or metabolic factors by the arterial wall. Our research is aimed at aquisition of information on the molecular restraints which define the resistance of a cell to proliferative stimuli. Specifically, we are concerned with the capability of the plasma low density lipoproteins to suppress mitogenesis. The aims of the proposed research are three: to isolate a homogeneous population of lipoprotein-sensitive cells, to characterize selected alterations of the cell membrane induced by membrane-bound plasma lipoproteins, and subsequently to discover how the alterations dictate cell function and response to external stimuli. This study focuses on the dual role of lipoproteins in regulating the phosphokinase system asssociated with the cell membrane and in determining the distribution of cell calcium ion and of the Ca+2-binding protein calmodulin. Our cellular targets are erythrocytes and lymphocytes which are relatively well-characterized and which may be studied in suspension culture. The rationale for the specific experiments proposed herein--a study focused on the ability of membrane-bound lipoproteins to regulate the phosphate content of membrane-associated myosin-like proteins--derives from evidence that contractile proteins, responsible for the dynamic structural organization of the cell, cycle between phosphorylated and dephosphorylated states.